The primate amygdaloid complex has long been identified as an important component of the brain system involved in mediating appropriate species-specific behaviors such as threat and defense. Large lesions of the inferior temporal lobe, which include the amygdala, produce the so called "Kluver-Bucy Syndrome" which has been characterized as an inability to attribute emotional significance to perceived stimuli. Critical reading of the literature, however, indicates that the experimental basis for this characterization remains tenuous. Previous studies have often suffered either from the lack of discrete lesions, comprehensive histological analysis or ethologically appropriate and sophisticated behavioral assessment. Moreover, recent studies in the human indicate that congenital impairment of amygdaloid function may be more debilitating to normal emotional and social interactions than lesions produced in the mature individual. The program of studies outlined in this revised application uses sophisticated neurobiological and behavioral methods to reassess the role of the primate amygdala in normal social interaction. The studies are carried out in the context of a long-standing program of neuroanatomical studies which demonstrate that the amygdala receives sensory information from widespread regions of the neocortex. The overarching hypothesis guiding this program is that the amygdala functions as a high level perceptual filter that interprets ongoing sensory information in order to orchestrate an appropriate species-specific response. The proposed studies will employ MRI-guided, axon-sparing stereotaxic ibotenic acid lesions of the amygdala along with the assessment of behavioral and physiological responses during dyadic and tetradic social interactions and videotape presentations. Behavioral data will demonstrate whether complete or partial amygdala lesions in the mature primate produce deficits in affiliative and/or agonistic behaviors. In a second phase of these studies, complete amygdala lesions will be produced in neonatal macaque monkeys. The effects of these lesions on mother-infant and juvenile-juvenile interactions will be evaluated. Future studies (when the neonates have matured) will analyze dyadic and tetradic social interactions and thus allow comparisons of the severity of effects of neonatal or mature amygdala lesions on social behavior. During these experiments, the pituitary-adrenal activation of lesioned and control monkeys in response to social and restraint stressors will also be analyzed. These studies will provide important insights into the neurobiology of normal social behavior and may contribute to an understanding of pathologies of social communication in disorders such as autism.